Public Library of Science
Browse
Figure_7.tif (366.68 kB)

EBNA3A contributes to the regulation of p16INK4A.

Download (0 kB)
figure
posted on 2010-06-10, 01:55 authored by Lenka Skalska, Robert E. White, Melanie Franz, Michaela Ruhmann, Martin J. Allday

(A) Western blot analysis of three LCLs established with virus derived from B95.8-EBV BAC (WT) and two established with EBNA3A-KO recombinants. The steady state levels of p16INK4A (p16) are elevated in the EBNA3A-KO cells relative to the WT-EBV infected cells. It should be noted that similar results were reported using a larger panel of EBNA3A-KO LCLs [8]. An LCL 3CHT (3CHT) with (+) or without (-) HT is shown for comparison. (B) & (C) ChIP analysis of H3K27me3 and H3K4me3 distribution on exon 1 (site C) and site A in the p16INK4A-ARF locus from an EBNA3A-KO LCL (3AKO) and a WT-EBV LCL (WT).

History

Usage metrics

    PLOS Pathogens

    Keywords

    Licence

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC